Tumor necrosis factor alpha and adalimumab differentially regulate CD36 expression in human monocytes 英文参考文献.docVIP

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Tumor necrosis factor alpha and adalimumab differentially regulate CD36 expression in human monocytes 英文参考文献.doc

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Tumor necrosis factor alpha and adalimumab differentially regulate CD36 expression in human monocytes 英文参考文献

Available online /content/9/2/R22 Research article Open Access Vol 9 No 2 Tumor necrosis factor alpha and adalimumab differentially regulate CD36 expression in human monocytes Jean Frédéric Boyer1,2,3, Patricia Balard1, Hélène Authier1, Bruno Faucon2, José Bernad1, Bernard Mazières3, Jean-Luc Davignon3,4, Alain Cantagrel2,3, Bernard Pipy1 and Arnaud Constantin2,3,5 1EA2405, Université Paul Sabatier, IFR31, BP84225, 31432 Toulouse CEDEX 4, France 2GRCB40, Université Paul Sabatier, IFR31, BP84225, 31432 Toulouse CEDEX 4, France 3Service de Rhumatologie, Centre Hospitalier Universitaire Rangueil, 1 avenue Jean Poulhès, 31059, Toulouse CEDEX 9, France 4INSERM, U563, IFR30, BP 3028, 31024 Toulouse CEDEX, France 5INSERM, U558, Faculté de Médecine, 37 allées Jules Guesde, 31073, Toulouse CEDEX 7, France Corresponding author: Arnaud Constantin, constant@cict.fr Received: 20 Nov 2006 Revisions requested: 11 Jan 2007 Revisions received: 12 Feb 2007 Accepted: 2 Mar 2007 Published: 2 Mar 2007 Arthritis Research Therapy 2007, 9:R22 (doi:10.1186/ar2133) This article is online at: /content/9/2/R22 ? 2007 Boyer et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract In chronic inflammatory diseases, such as rheumatoid arthritis, inflammation acts as an independent cardiovascular risk factor and the use of anti-inflammatory drugs, such as anti-tumor necrosis factor alpha (anti-TNFα), may decrease this risk. The phagocytosis of oxidized low density lipoproteins (LDLs) accumulated in the subendothelium by mononuclear cells influences atherosclerosis and depends on CD36 expression. We investigated the role of TNFα and adalimumab, a human monoclonal antibody widely used in human pathology,